An information resource for serving & former members of the Irish Army Air Corps suffering illness due to unprotected toxic chemical exposure in the workplace.
Background: In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) completed a toxicological review of trichloroethylene (TCE) in September 2011, which was the result of an effort spanning > 20 years.
Objective
We summarized the key findings and scientific issues regarding the human health effects of TCE in the U.S. EPA’s toxicological review.
Methods
In this assessment we synthesized and characterized thousands of epidemiologic, experimental animal, and mechanistic studies, and addressed several key scientific issues through modelling of TCE toxicokinetics, meta-analyses of epidemiologic studies, and analyses of mechanistic data.
Discussion
Toxicokinetic modelling aided in characterizing the toxicological role of the complex metabolism and multiple metabolites of TCE. Meta-analyses of the epidemiologic data strongly supported the conclusions that TCE causes kidney cancer in humans and that TCE may also cause liver cancer and non-Hodgkin lymphoma. Mechanistic analyses support a key role for mutagenicity in TCE-induced kidney carcinogenicity.
Recent evidence from studies in both humans and experimental animals point to the involvement of TCE exposure in autoimmune disease and hypersensitivity.
Recent avian and in vitro mechanistic studies provided biological plausibility that TCE plays a role in developmental cardiac toxicity, the subject of substantial debate due to mixed results from epidemiologic and rodent studies.
Conclusion
TCE is carcinogenic to humans by all routes of exposure and poses a potential human health hazard for noncancer toxicity to the central nervous system, kidney, liver, immune system, male reproductive system, and the developing embryo/fetus.
Evaluate the toxic effects of Aqueous Film-Forming Foams used by firefighters for Class B fire suppression in human-derived kidney cells (HEK-293).
Methods
Three widely used AFFFs were collected from fire departments and were added to HEK-293 cells in various concentrations. Seventy-two hours post-treatment, cellular proliferation and toxicity were examined using commercially available kits.
Results
All AFFFs evaluated induced cellular toxicity and significantly decreased cell proliferation, even when cells were treated with concentrations 10-fold lower than the working concentration used for fire suppression.
Conclusion
Despite the reduced usage of PFAS-containing AFFFs in the firefighter work environment, the evaluated AFFFs demonstrated significantly altered cellular proliferation, while also inducing toxicity, indicating the presence of toxic compounds. Both stronger implementation of PFAS-containing AFFFs restrictions and robust evaluation of fluorine-free and next-generation AFFFs are warranted.
In Brief
Firefighters are routinely exposed to per- and polyfluoroalkyl substances (PFAS) through the use of Aqueous Film-Forming Foams (AFFFs) for the suppression of Class B fire, which derive from flammable and combustible liquids, such as gasoline and alcohol. The addition of surfactants and PFAS in the AFFFs allows them to form an aqueous film that can extinguish the fire, while also coating the fuel. As such, AFFFs are often used for fire extinction in airports and military bases.
Exposure to PFAS in the general population may arise from ingestion of contaminated food or water, usage of consumer products containing PFAS, such as non-stick cookware or stain resistant carpets and textiles, and inhalation of PFAS-containing particulate matter. Detection of increased serum PFAS concentrations has been linked to an elevated risk for kidney cancer in humans, and firefighters are known to have increased serum concentrations of certain PFAS after attending training exercises. In the same study it was also observed that the average urinary excretions of 2-butoxyacetic acid (2-BAA) a surfactant often added in AFFFs exceeded the reference limit of the occupationally unexposed population, ranging from 0.5 to 1.4 mmol/mol creatinine.
Furthermore, an increased risk of mortality from kidney cancer has been observed in firefighters compared to the U.S. population. The detrimental health effects of PFAS are exacerbated by their increased half-lives in humans. A recently published study examined the half-lives of short- and long- chained PFAS in the serum of 26 airport employees and observed a wide range of half-lives which was dependent on the length and chemical structure of each substance that was examined. Indicatively, the shortest half-life was described for perfluorobutanesulfonic acid (PFBS), while the linear isomer of perfluorooctanesulfonic acid (PFOS) had the longest half-life (average of 44 days and 2.93 years, respectively), findings which are in agreement with other sources in the literature.
One aspect of this phenomenon could be attributed to renal reabsorption, as humans actively transport PFAS in the proximal tubules. A recently published scoping review of 74 epidemiologic, pharmacokinetic, and toxicological studies examined the relationship between PFAS exposure and kidney-related health outcomes. It was observed that exposure to PFAS was associated with lower kidney function, including chronic kidney disease (CKD), and histological abnormalities in the kidneys, as well as alterations in key mechanistic pathways, that can induce oxidative stress, and metabolic changes leading to kidney disease.
The alarming number of studies showcasing the harmful health effects pertaining to PFAS exposure has led to the banning of the production of AFFFs containing highly toxic, long chain PFAS, such as perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) since 2015. However, this regulation is gradually being implemented across states and little is known about the toxicity of the next generation AFFFs. Based on the above, in the present study we evaluate cellular proliferation and toxicity in kidney-derived cells (HEK-293) that were exposed to three widely used AFFFs.
Photo of dichloromethane (DCM) as stored by Irish Air Corps in 2015. DCM was banned in the EU in 2012.
Objective
We hypothesize that different sources of lung irritation may contribute to elicit an immune reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic susceptibility to the disease. We aimed to investigate the influence of exposure to organic solvents on MS risk, and a potential interaction between organic solvents and MS risk human leukocyte antigen (HLA) genes.
Methods
Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947 controls), participants with different genotypes, smoking habits, and exposures to organic solvents were compared regarding occurrence of MS, by calculating odds ratios with 95% confidence intervals using logistic regression. A potential interaction between exposure to organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.
Results
Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence interval 1.2–1.8, p = 0.0004). Among both ever and never smokers, an interaction between organic solvents, carriage of HLA-DRB1*15, and absence of HLA-A*02 was observed with regard to MS risk, similar to the previously reported gene-environment interaction involving the same MS risk HLA genes and smoke exposure.
Conclusion
The mechanism linking both smoking and exposure to organic solvents to MS risk may involve lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes argues for an action of these environmental factors on adaptive immunity, perhaps through activation of autoaggressive cells resident in the lungs subsequently attacking the CNS.
Anecdotal evidence has been emerging for some time of potential illness clusters at Casement Aerodrome to which Multiple Sclerosis has now been added. We are calling for these potential clusters to be investigated by competent authorities.
According to the World Health Organization (WHO), seven million people worldwide die as a consequence of air pollution every year. For around 20 years, studies have shown that air-borne particulate matter negatively affects human health. Now, in addition to already investigated particle sources like emissions from heating systems, industry and road traffic, aircraft turbine engine particle emissions have also become more important.
Photo of Alouette III No 196 showing soiling of the tail boom with soot from exhaust gasses.
In a unique, innovative experiment, researchers have investigated the effect of exhaust particles from aircraft turbine engines on human lung cells.
The cells reacted most strongly to particles emitted during ground idling.
It was also shown that the cytotoxic effect is only to some extent comparable to that of particles from gasoline and diesel engines.The primary solid particles, i.e. those emitted directly from the source, have the strongest effect on people in its immediate vicinity.
Now a multidisciplinary team, led by lung researcher Marianne Geiser of the Institute of Anatomy at the University of Bern, together with colleagues from Empa Dübendorf and the University of Applied Sciences and Arts Northwestern Switzerland (FHNW), has shown that primary soot particles from kerosene combustion in aircraft turbine engines also cause direct damage to lung cells and can trigger an inflammatory reaction if the solid particles are inhaled in the direct vicinity of the engine.
The researchers demonstrated for the first time that the damaging effects also depend on the operating conditions of the turbine engine, the composition of the fuel, and the structure of the generated particles.
Beechcraft 200 Super King Air No 240 showing soiling of the engine panels with soot from exhaust gasses.
Extremely small particles in the nanoscale range
Particles emitted from aircraft turbine engines are generally ultrafine, i.e. smaller than 100 nm. By way of comparison, a human hair has a diameter of about 80,000 nm. When inhaled, these nanoparticles — like those from other combustion sources -efficiently deposit in the airways. In healthy people, the well-developed defense mechanisms in the lungs normally take care of rendering the deposited particles ineffective and removing them from the lungs as quickly as possible.
However, if the inhaled particles manage to overcome these defense mechanisms, due to their structure or physico-chemical properties, there is a danger for irreparable damage to the lung tissue. This process, already known to researchers from earlier experiments with particle emissions from gasoline and diesel engines, has now also been observed for particle emissions from aircraft engines.
Toxicity depends on the operating conditions of the turbines and the type of fuel
Evidence of increased cell membrane damage and oxidative stress in the cell cultures was identified. Oxidative stress accelerates ageing of cells and can be a trigger for cancer or immune system diseases.
Overall, according to the researchers, it has been demonstrated that the cell-damaging effect caused by exposure to particles generated by the combustion of gasoline, diesel and kerosene fuel are comparable for similar doses and exposure times.
Additionally, a similar pattern was found in the secretion of inflammatory cytokines after exposure to gasoline and kerosene fuel particles.
Aerosols: distance from the source is crucial
Aerosols are the finest solid or fluid substance suspended in the air. In combustion processes, the composition of ultrafine particles is highly variable. In addition, aerosols are unstable, and they are modified after their formation. Primary ultrafine solid particles have a high diffusion velocity. As a result, at high concentrations such particles either stick together or attach to other particles. Therefore, the effect of primary ultrafine particles depends on the distance from the source, implying that there is a difference depending on whether a person is close to the source (such as people at the roadside ) or at a greater distance (aircraft taxiing or taking off). Further research is needed to clarify how strong the impact would be at a greater distance from an aircraft engine
The layout of the Irish Air Corps base at Casement Aerodrome ensures that aircraft exhaust gasses are blown over populated sections of the airbase when winds are from the south, south east or south west. This includes hangars, offices, workshops and living in accommodation such as the apprentice hostel and married quarters. Calm weather also creates conditions where exhaust gasses linger in higher concentrations.
This results in all Irish Air Corps personnel (commissioned, enlisted, civilian & family) being exposed to emissions from idling aircraft engines, emissions that are known to cause harm.
In the mid 1990s a study of air pollution adjacent to the ramp area at Baldonnel was commissioned. This report relating to this study has gone missing.
Anecdotal evidence suggests increased prevalence of occupational asthma & adult onset asthma amongst serving & former personnel who served in Baldonnel or Gormanston aerodromes.
Older gas turbine engines produce dirtier exhaust gasses.
Idling gas turbine engines produce dirtier exhaust gasses.
Below are some of the gas turbine powered Air Corps aircraft that were powered by elderly engine designs.
Royal Australian Air Force (RAAF) personnel who worked with widely used jet fuel suffered damage to their body’s cells with unknown long-term consequences, according to groundbreaking research released after a Freedom of Information laws request.
Defence’s senior physician in occupational and environmental medicine, Dr Ian Gardner, described the findings as a “part of the puzzle” and a hypothesis-making study”, and pointed it out that it was one of a series of pieces of research currently underway.
“What it shows is there is evidence of small but persistent cellular damage,” Dr Gardner told the ABC. He said it was not yet clear what the long-term effects of that damage might be.
“For the future though there are a lot of other aircraft maintenance workers who have done similar jobs on other aircraft types, and now Defence and DVA and Air Force are considering what additional work should be done in relation to those other people who are not actually on the F-111 programs but have done essentially similar work,” Dr Gardner said.
The Jet Fuel Syndrome Study also shows that the fuel is more toxic to the body’s cells than the two solvents initially blamed for the sickness suffered by the deseal/reseal workers, and that the toxicity is even higher when those solvents and the fuel were mixed.
The results of the research project, headed by Professor Francis Bowling of Brisbane’s Mater Hospital, were handed to Defence last September, and have been the subject of significant scrutiny and review due to the potential significance of the findings.
They will give heart to former and serving Defence personnel who believe they have been left out in the cold by Defence after developing serious health complaints while working with fuel and other substances.
Junior Minister with responsibility for Defence said in the Dáil that he was assured by the Irish Air Corps that the RAAF F1-11 deseal/reseal exposure tragedy is completely different to any exposures at the Irish Air Corps.
Was the minister suggesting that Irish Air Corps gas turbine engines don’t run on jet fuel?
As the world frantically battles coronavirus, a leading Dutch neurologist warns of the next global pandemic — and this one, he says, is almost entirely of our own making.
Bastiaan Bloem, MD, a neurologist and professor at Radboud University Nijmegen Medical Center, says that over the next 20 years, the number of people with Parkinson’s disease (PD) will likely double — from the present 6.5 million to more than 13 million.
The main cause of this exponential jump: widespread exposure to herbicides, solvents, and other toxic chemicals used in agriculture and manufacturing.
“A pandemic, as everybody is now painfully aware, is a disease happening worldwide, to which no one is immune. PD fulfills all those criteria,” Bloem told Parkinson’s News Today in a phone interview from the Netherlands.
“Parkinson’s is now the fastest-growing neurological condition on the planet.”
Bloem, 53, points to the tight link between exposure to herbicides such as paraquat — a weed killer — and the risk of developing Parkinson’s.
“These chemicals were introduced worldwide after World War II, and many are still used today on our fields,” he said. “For this reason, farmers are at a markedly increased risk of developing Parkinson’s. If you feed a mouse paraquat — which is banned in China but not the U.S. — it will kill the dopamine-producing cells in the brain. These chemicals are tremendously toxic to the brain and have even been detected in milk, in supermarkets.”
Paraquat isn’t the only such chemical posing this risk. Trichloroethylene, a solvent used to clean metals and remove stains, has exactly the same effect on human brains. Yet it’s still widely used and is detectable in high concentrations in groundwater, he said.
“Parkinson’s is exploding in numbers, it’s a horribly debilitating disease, and it’s a costly disease that should matter to people and governments. We’re doing this to ourselves,” Bloem said. “But we can do something about it. We need to get rid of these toxic pesticides and move toward organic food. And we should take measures to protect people who work in these toxic environments.”
Trichloroethylene was used in Baldonnel for decades with ERF in particular receiving it in 220 litre drums. From ERF it was handed out without any precautions or training to anyone who asked for it. It was handed out in milk cartons, plastic coke bottles etc.
Trichloroethylene was used by all hangars & workshops in an ad-hoc basis usually with Trichloroethylene begged from ERF although some units did order it themselves. Personnel in the Air Corps museum also used Trike to help degrease parts & aircraft being restored for the museum.
Trichloroethylene was also used by both apprentices, tech & line personnel to carry out cleaning tasks in the Air Corps Training Depot while on training courses or during “war week”.
In at least 2 separate instances some floors in ACTD were completely destroyed by the use of Trichloroethylene being left overnight to clean them. In one incident Trichloroethylene dissolved through a traditional lino floor as far as the backing twine and in another incident few years later a tiled floor was destroyed after the tiles shriveled up & shrunk after Trichloroethylene was left overnight to clean a floor.
Trichloroethylene was also used by teenage apprentices to clean black marks off floors in the Apprentice Hostel and the Apprentice School.
At no point was anyone ever given training in the use of Trichloroethylene nor issued with appropriate PPE whilst working with the chemical.
A number of Irish Air Corps personnel have been diagnosed with early onset Parkinson’s disease
Concerns related to adverse health effects experienced by aircrew exposed to aircraft contaminated air have been ongoing for over 6 decades.
Unfiltered breathing air is supplied to the cabin via the engine compressor. The likelihood that oil leaking over the engine oil seals may enter the cabin air supply has prompted continuing debate about the hazards associated with exposure to neurotoxic substances and to the thermally degraded or pyrolysed mixture.
In this study, we undertook an in-depth investigation of aircrew involved in suspected aircraft contaminated air events.
Methods
Two studies were conducted to review the circumstances and symptoms of a cohort of aircrew working in the pressurized air environment of aircraft. A table of effects was then used for categorizing symptoms and reviewing other sources of data related to aircraft fluids and selected other conditions.
Results
Both acute and chronic exposures to neurotoxic and a wide range of thermally degraded substances were confirmed, along with a clear pattern of acute and chronic adverse effects. The latter were supported by medical findings and diagnoses, notably involving the neurological, neurobehavioural and respiratory systems.
Conclusion
A clear cause and effect relationship has been identified linking the symptoms, diagnoses and findings to the occupational environment. Recognition of this new occupational disorder and a clear medical investigation protocol are urgently needed.
Engine bearing oil leak on compressor blades in CFM56-7 engine on a Boeing 737. This oil leak was within acceptable manufacturer limits and this engine is still fully serviceable.Yep we know the Irish Air Corps don’t have any 737 aircraft but this Boeing Aircraft Maintenance Manual shows engine bearing compressor oil leaks are routine and don’t necessarily cause the engine to become U/S.
Download scientific research paper from the World Health Organisation…
We are curently updating our chemical listings. There were and are a very large number of chemical substances in use in the Irish Air Corps and amost all of these substances have ingredient chemicals.
For example, the corrosion inhibiter Mastinox 6856k, which many personnel used without any PPE, contains the below constituent chemicals. Among the ingredients include carcinogens, mutagens, immune sensitisers, irritants and just plain old toxic chemicals.
Strontium Chromate
Barium Chromate
Xylene
Toluene
Ethylbenzene
By following the links below you will arrive at tables showing the individual chemical names that we have extracted from some MSDS. Due to a recent Supreme Court ruling the list of chemicals is expected to grow. It is our intention to eventually create a database that links the MSDS to the individual constituents.
Bear the following in mind when using the table.
You can limit the number of entries you want to see
You can search for names such as “Tolouene” or “chromate”
You can sort by name, carcinogen, mutagen, reprotoxic etc.
Clicking on the name will take you to the Wikipedia page for that chemical
Clicking on the ECHA link for a chemical will take you to the European Chemicals Agency where you can look at the hazards in detail and view CAS number etc.
The tables do SCROLL sideways, the scroll bar is at the bottom of each table.
Consider the trappings of modern life: Calvin Klein Eternity, gasoline, Gore-Tex, hairspray, paint, particle board, polyurethane iPod cases.
Now imagine that you’re allergic to virtually all of them.
Environmentalists usually think about chemical toxicity as either a dramatic local crisis (Bhopal, Love Canal) or the simmering concern of those far away (breast-feeding mothers in the Arctic) or far in the future (our oft-evoked grandchildren). But for people suffering from Multiple Chemical Sensitivities, the chemical crisis is already here. Indeed, thanks to industrialisation, it is already everywhere. And, like so many environment-related health issues, it disproportionately affects the poor and, moreover, drives many once financially stable people into poverty.
As a disease, Multiple Chemical Sensitivities doesn’t have an official case definition yet (more on this soon), but rather refers to a broad range of adverse symptoms brought on by an even more broad array of everyday chemicals. These symptoms are often provoked at exposure levels far below those that seem to affect the rest of the population — levels virtually always present in our homes, workplaces, and social venues. They commonly include severe headaches, food intolerance, difficulty breathing, nausea, irritation of the eyes, ears, nose, throat, and skin, and disorientation or confusion, but there are many more.
Current theories range from a genetic predisposition to chemical injury, to neurological damage, to abnormalities in detoxifying enzymes, to a so-called “toxicant-induced loss of tolerance” to environmental stressors, in which one particular exposure to a toxic substance overwhelms a person’s system and leaves them unable to cope with exposures to a wide range of other toxins.
It can be even more difficult finding an MCS-safe job. Even if a workplace itself is a tolerable environment (rare, given the ubiquity of toxic building materials), basic job-related interactions with the general public can be impossible. “The way a typical story goes,” says Zwillinger, “is that people lose the ability to make a living because they can’t be out in the public arena” without getting ill. Some MCS patients find a way to work from home (assuming they’ve found safe housing) — but that option is seldom available to poorer Americans forced to rely on low-wage, low-skill jobs.
It’s a bitter irony, since many with MCS see themselves as canaries in the modern-day coal mine. As recently as 1986, the exquisitely sensitive yellow birds were used to detect the presence of dangerous gases in mine shafts, and when they showed signs of illness — when they ceased to sing — it was an unambiguous warning: evacuate.
As growing numbers of MCS sufferers are driven from their homes and jobs, pushed to the fringes of medical science and the brink of financial ruin, made sick by industrialised civilisation itself, we would do well to heed their equally urgent warning. And fast, because this time around we can’t evacuate. There’s nowhere else to go.
Air Corps Chemical Abuse Survivors are the canary in the coalmine for inflammatory illness being caused by ubiquitous chemical exposure in our home, work, vehicles, food & clothing.
The appalling high concentration chemical exposure suffered by Air Corps personnel caused chemical related illnesses in young fit men & women in a very short space of time making us a very valuable cluster for medicine & science to study.
Study us, fix us and there will be a public health dividend.
